Abstract

Cumulative mortalities of 100, 50, 20, and 0% due to gas bubble disease (GBD) occurred on exposure of rainbow trout (Salmo gairdneri) for 180 min to supersaturated water at 136, 130, 124, and 116% total dissolved gas saturation (TDGS), respectively. At 130% TDGS, a prior exposure to carbon monoxide (CO), which converted 80% of the hemoglobin to carboxyhemoglobin (COHb), significantly prolonged survival time, but cumulative mortality was insignificantly reduced in the same group. Histologically, all supersaturation mortalities had branchial lesions for GBD (characterized by gas displacement of blood from the afferent arterioles of the gill filaments), while 70% had gas emboli in the retinal choroid gland. At a TDGS of 100%, these histological lesions were not observed and the CO 80% COHb conversion did not induce mortality within 120 min. Breathing movements of both control and CO-exposed fish slowed greatly when a TDGS of 130% was imposed; however, the COHb conversion initiated tachypnea and the CO-treated fish maintained a relatively higher respiratory rate when exposed to supersaturation conditions for a period which was proportional to their prolonged survival time. We concluded that the initial formation of gas emboli preceding fatal GBD was delayed as a result of a CO-inhibited function of hemoglobin.

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